Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2003-12-3
pubmed:abstractText
Repeated treatments with neuroleptics are associated with biochemical and morphological alterations in forebrain neurons as well as an upregulation of D2-mediated changes in neuronal function. The present study evaluated the histological and physiological effects of three once-daily treatments with two chemically divergent neuroleptics, haloperidol (1 mg/kg i.p./day) and eticlopride (3 mg/kg i.p./day), measured in rats 24 h after the last injection. It was determined that this short-term antagonism of D2-like receptors induced fiber and terminal degeneration and significantly decreased tyrosine hydroxylase (TH) and brain-derived neurotrophic factor (BDNF) immunoreactivity in the ventral pallidum (VP), as determined by optical density measurements. While other forebrain regions demonstrated changes in TH and BDNF, the neurodegeneration profile was unique to the VP. This was accompanied by an enhancement in the efficacy of the D2 agonist quinpirole to increase spiking rate of VP neurons recorded in chloral hydrate-anesthetized rats. These data indicate that short-term treatments with D2 antagonists are sufficient to induce changes in the biochemical and morphological profiles uniquely within the VP. Moreover, the functional ramifications of these changes appear to include profound alterations in the way dopamine regulates neuronal activity in this region.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
2
pubmed:volume
995
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
14-22
pubmed:meshHeading
pubmed-meshheading:14644466-Animals, pubmed-meshheading:14644466-Antipsychotic Agents, pubmed-meshheading:14644466-Brain-Derived Neurotrophic Factor, pubmed-meshheading:14644466-Cell Survival, pubmed-meshheading:14644466-Disease Models, Animal, pubmed-meshheading:14644466-Dopamine, pubmed-meshheading:14644466-Dopamine Agonists, pubmed-meshheading:14644466-Dopamine Antagonists, pubmed-meshheading:14644466-Drug Administration Schedule, pubmed-meshheading:14644466-Dyskinesia, Drug-Induced, pubmed-meshheading:14644466-Haloperidol, pubmed-meshheading:14644466-Immunohistochemistry, pubmed-meshheading:14644466-Male, pubmed-meshheading:14644466-Microscopy, Electron, pubmed-meshheading:14644466-Nerve Degeneration, pubmed-meshheading:14644466-Presynaptic Terminals, pubmed-meshheading:14644466-Prosencephalon, pubmed-meshheading:14644466-Quinpirole, pubmed-meshheading:14644466-Rats, pubmed-meshheading:14644466-Rats, Sprague-Dawley, pubmed-meshheading:14644466-Receptors, Dopamine D2, pubmed-meshheading:14644466-Salicylamides, pubmed-meshheading:14644466-Synaptic Transmission, pubmed-meshheading:14644466-Tyrosine 3-Monooxygenase
pubmed:year
2004
pubmed:articleTitle
Short-term, D2 receptor blockade induces synaptic degeneration, reduces levels of tyrosine hydroxylase and brain-derived neurotrophic factor, and enhances D2-mediated firing in the ventral pallidum.
pubmed:affiliation
Department of Cellular and Molecular Pharmacology, The Chicago Medical School, Finch University of Health Sciences, 3333 Green Bay Rd., North Chicago, IL 60064-3095, USA. Gloria.Meredith@finchcms.edu
pubmed:publicationType
Journal Article